Abstract
Human platelet antibody (HPA) detection is necessary for the diagnosis and therapeutic decisions for refractoriness to platelet transfusions, post transfusion purpura and fetal and neonatal alloimmune thrombocytopenia. In the last four to five decades many new developments, both in knowledge and methods, have increased the quality of platelet serology. However, the quest for the optimal antibody detection method(s) encountered, sometimes unexpected, difficulties. In this review the various aspects concerning platelet antibody test methods and detection of platelet antibodies both for the diagnostic and screening setting are discussed.
Highlights
Human platelet antibody (HPA) detection is necessary for the diagnosis and therapeutic decisions for refractoriness to platelet transfusions, post transfusion purpura and fetal and neonatal alloimmune thrombocytopenia
Major drawbacks of these whole platelet assays are the co-expression of human leucocyte antigen (HLA)class-I antigens and Fc-gamma-receptor (FcγR)IIa on platelets causing difficulties to distinguish HLA antibodies from human platelet antigen (HPA) antibodies and non-specific binding of IgG via the Fc-part to the Fc-receptor
In a Dutch 10-years external quality assessments (EQA) overview [66], we provided some clarity about the value of various techniques for the detection of platelet antibodies
Summary
Methods (phase I) for platelet antibody detection such as platelet aggregation tests, serotonin release and complement fixation techniques made use of the functional properties of blood platelets for indirect evidence for the presence of antibodies [1,2,3,4,5]. In the 1970s the availability of radiolabelled or immune fluorescence labelled anti-human immunoglobulins of the IgG, IgM or IgA class led to the development of more sensitive and specific methods (phase II) e.g. radio immune assay (RIA), platelet immunofluorescence test (PIFT) and mixed passive haemagglutination assay (MPHA) [7,8,9,10,11,12,13,14,15,16] With these assays, detection of antibody binding on donor platelets incubated with serum from the patient (indirect method) or directly on patient platelets (direct method) became possible. Chloroquine removes the HLA antigens from the platelet surface and prevents HLA antibodies from binding while the human platelet antigens carrying glycoproteins remain intact [17,18,19]
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